Feline infectious peritonitis (FIP) is a sporadic disease occurring unpredictably in domestic and wild Felidae. While FIP is primarily a disease of domestic cats, it has been diagnosed in lions, mountain lions, leopards, cheetahs, and the jaguar. Smaller wild cats that have been afflicted with FIP include the lynx and caracal, sand cat, and pallas cat. In domestic cats, the disease occurs predominantly in young animals, although cats of all ages are susceptible. A peak incidence occurs between 6 and 12 months of age. A decline in incidence is noted from 5 to 13 years of age, followed by an increased incidence in cats 14 to 15 years old. There is no significant sex predisposition. FIP occurs more frequently in purebred cats, presumably because these cats are kept more commonly in catteries or multiple cat households. The disease is world-wide in distribution.
FIP is caused by a type of coronavirus. Coronaviruses are pleomorphic, enveloped particles that average 100 nm in diameter and contain a single strand of RNA. Characteristic petal-shaped projections called peplomers pronude from the viral surface. In many species of animals, coronaviruses have a relatively restricted organ tropism, infecting the respiratory and/or gastrointestinal systems. Following oral infection, the viruses have an affinity for the mature apical columnar epithelium of the villi in the duodenum, jejunum, and ileum.
The coronaviruses that infect cats have been divided into those that cause FIP (FIPVs) and those that induce subclinical to severe enteritis (the feline enteric coronaviruses, or FECVs). The FIPVs differ from the FECVs in theft ability to escape from the gastrointestinal tract and spread to replication sites in distant tissues. FIPVs and FECVs may represent pathogenetic variants of a single coronavirus type. Alternatively, FIPVs may arise periodically as mutants of FECV strains.
FIPV, transmissible gastroenteritis virus (TGEV) of swine, canine coronavirus (CCV), and human respiratory tract coronaviruses of the 229E group comprise an antigenic cluster of closely related viruses within the Coronaviridae group. The major structural polypeptides of FIPV, TGEV, and CCV are so similar antigenically that some consider these three viruses as host range mutants rather than individual viral species.
The name, feline infectious peritonitis, refers to the principal form of the disease, an inflammatory condition of the visceral serosa and omentum. A reported second form of FIP is characterized by granulomatous involvement of parenchymatous organs such as the kidneys, mesenteric lymph nodes, liver, pancreas, central nervous system (CNS) and spine, and the uveal tract of the eye. The granulomatous form of FIP is called "dry" or "noneffusive" because there is no inflammatory exudation into the body cavities. Classical FIP, which comprises about three-fourths of the cases, is termed "wet" or "effusive." A third form of FIP combines characteristics of both the effusive and noneffusive varieties.
The clinical course of effusive FIP lasts from 1 to 6 weeks or sometimes longer. The onset of disease is heralded by the appearance of a chronic, fluctuating fever. Associated with the fever there is usually a progressive decline in weight, activity, and appetite. Terminally, the cats go into shock and die. Peritonitis is seen in over 90% of the cats with effusive FIP and pleuritis in around 40% of the cases. Involvement of other organs, such as the eyes and CNS, is clinically apparent in only 10% of the cats with effusive disease, although a somewhat higher proportion may have clinically silent lesions in these and other non-serosal sites.
Cats with noneffusive FIP are ordinarily ill for 1 to 12 weeks or longer. As with the effusive form, a chronic fluctuating fever accompanies the disease. There also is a progressive decline in general body condition and appetite. Added to these features, however, are signs referable to specific organ systems. Peritoneal cavity lesions are found in 50% of cats with noneffusive FIP and pleural cavity lesions in 10%. Noneffusive FIP differs from the effusive form in that there is a high incidence of ocular or CNS involvement. Approximately one-third of cats with noneffusive FIP demonstrate signs referable to the CNS, and a similar number have clinically-apparent ocular disease.
The precise routes by which FIPV enters the body are not known. FIPV is a heat-labile virus, being inactivated at room temperature within 24 to 48 hours. It is unlikely that cats with FIP are the only source of FIPV in nature. Similarly, contaminated fomites are an unlikely source of infection, given the short stability of FIPV outside the host. In most cases, transmission of virus probably occurs via the feces and, less commonly, the urine or oronasal secretions of asymptomatic carriers. To explain the sporadic and random incidence of the disease, carder cats would have to shed the virus either intermittently or at exceedingly low levels.
Queens that are asymptomatically infected with FIPV may infect their offspring in-utero or in the neonatal period. Kittens infected in-utero may be born sick or may show no signs of disease. However, some asymptomatic infected kittens may develop FIP at a later time if their immune responsiveness becomes impaired.
Concurrent infection with feline leukemia virus (FeLV) has been reported in cats infected with FIPV. The mechanism by which FeLV infection potentiates the incidence of FIPV is not specifically known, although controlled observations reported in the literature have led to the assumption that FeLV infection in some way interferes with established FIPV immunity. The mechanism of this interference has been speculated to involve any number of generalized immunosuppressive effects that have been described in connection with persistent FeLV infection, which dispose cats to intercurrent or opportunistic infections.
Specific pathogen-free (SPF) kittens that are exposed to FIPV by oral or intratracheal instillation react serologically in several ways. Some kittens do not develop any signs of infection after prolonged exposure, and they remain antibody-negative. Kittens which are infected but do not develop signs of illness demonstrate a plateau-shaped antibody response, while kittens that develop FIP demonstrate a progressive antibody titer rise. In both groups of infected kittens, the presence of virus-neutralizing antibodies tends to correlate with immunofluorescent antibody (IFA) titers. Sometimes, however, an infected cat will develop only virus-neutralizing antibodies, and IFA tilers will be negligible. Difficulty is encountered in the interpretation of serologic responses due to antigenic similarity between FIPV and the non-FIP-inducing coronaviruses (FECV), and the ubiquitousness of FECV infection in nature. About 25% of free-roaming cats have been or remain infected with FECV, with infections especially prevalent in catteries and multiple cat households. Infection with FECV results in the production of coronaviral antibody that is, at present, serologically indistinguishable from that induced by infection with FIPV, CCV, or TGEV.
Antibody formed as a result of FECV infection does not protect the cat from later challenge with a virulent strain of FIPV. In fact, this antibody sensitizes the cat to later challenge, accelerating the disease process induced by the virulent FIPV.
Initial attempts to immunize cats with TGEV of swine to provide protection against FIP have proven unsuccessful, although immunization of piglets with FIPV is known to invoke antibody production against TGEV. To date, immunization with killed FIPV also has proven uniformly unsuccessful. The immunity derived from autologous killed vaccines almost always renders cats more susceptible to challenge with the virulent living virus, and the disease that results usually is more severe and fulminating. Vaccination with attenuated FIPV also has proven unsuccessful as evidenced by a lack of such products commercially. In this regard, reference is made to Gerber et al, "Protection Against Feline Infectious Peritonitis by Intranasal Inoculation of a Temperature-Sensitive FIPV Vaccine", Vaccine, Vol. 8, pp 536-542 (December 1990); and U.S. Pat. Nos. 4,293,653, 4,303,644, and 4,571,386.
The prognosis for cats with FIP is poor, since there is currently no effective treatment to terminate the viral infection. Some treatment regimens allow short-term remissions in carefully selected patients. The best patients for palliative therapy are those cats with FIP that are not infected with FeLV, are in good physical condition, maintain a good appetite, and have no evidence of severe anemia or neurologic signs. Unfortunately, few cats with FIP are presented early enough in the course of disease to meet these criteria, and most afflicted cats will die within 1 to 16 weeks.
Sources of additional information concerning FIP include Olsen et al., Comparative Pathobiology of Viral Diseases, vol.2, pp.115-136, CRC Press, Inc., Boca Raton, Fla. (1985), and references cited therein; and Norden News, Autumn 1989, pp.15-19, Lincoln, Nebr., the disclosures of which are incorporated expressly herein by reference.